The neuroanatomical substrate for mammalian photoperiodism remains unknown, although it is generally believed that the melatonin "readout system" which distinguishes long-photoperiod from short-photoperiod melatonin patterns, and modulates luteinizing hormone-releasing hormone (LHRH) secretion accordingly, is located within the hypothalamus. In the present study, this assumption was tested in male hamsters by placing bilateral lesions in an extrahypothalamic region of the brain, namely the bed nucleus of the stria terminalis (BNST), and monitoring the animals' subsequent ability to regress their testes after transfer from long photoperiods (14L:10D) to short photoperiods (6L:18D). After 15 weeks of exposure to short photoperiods, sham-lesioned hamsters showed the expected level of testicular regression (mean testicular weight 0.471g); hamsters maintained under long photoperiods typically have testes that weigh approximately 3 g. A similar level of testicular regression was shown by hamsters which had been lesioned dorsally to the BNST (mean testicular weight 0.452g). In contrast, the level of testicular regression was significantly blocked in hamsters which had been lesioned within the BNST (mean testicular weight 2.577g). These data are compatible with previous reports demonstrating that removal of the olfactory bulbs blocks short-photoperiod-induced testicular regression (i.e., the olfactory bulbs project to the BNST). Moreover, the data suggest that a locus within the BNST plays a key role in photoperiodism and may function as a "comparator," which integrates photoperiodic information from the primary melatonin-sensitive system and relays it to the neural circuits that control LHRH secretion. As in the hamster, the activity of reproductive axis in primates can also be modulated, to some extent, by photoperiodic manipulations. Therefore, these findings should help to disclose common inhibitory neural circuits that play a key role in the etiology of centrally-originating human reproductive disorders.